Music often evokes strong emotions, such as excitement, joy, and nostalgia. These emotions can be highly pleasurable and accompanied by increased physiological arousal. Pleasure-inducing music activates a network of brain regions including the medial prefrontal cortex (mPFC), striatum, and amygdala. In Experiment 1, I explore the neural structures critical for music-evoked pleasure. I hypothesize that individuals with damage to brain regions involved in emotional responses to music (e.g., mPFC, striatum, amygdala) will show a decrease in their pleasurable responses to music after brain injury. Patients from the Iowa Neurological Patient Registry completed questionnaires that assessed current emotional responses to music and changes in emotional responses to music after brain injury. The results provided partial support for the hypothesis, and the most striking loss of musical pleasure (referred to as "music anhedonia") occurred in a patient with damage to the striatum. However, musical pleasure appears to be relatively resistant to brain damage, as music anhedonia was only observed in a few individuals with varying regions of brain damage.
Along with strong emotions, music often triggers distant memories. However, the mechanism underlying music-evoked autobiographical memories (MEAMs) has not yet been investigated. Here, I predict that emotion is a central aspect underlying MEAMs. In Experiment 2a, I tested the hypothesis that MEAMs are more emotional and vivid than autobiographical memories evoked by pictures of famous faces. Neurologically normal, healthy adults viewed pictures of famous faces and listened to music while electrodermal activity was recorded. After each stimulus, participants described any memories that were evoked. Supporting my prediction, I found that MEAMs were significantly more vivid than face-evoked memories. In addition, music that evoked memories was accompanied by increased skin conductance responses compared to music that did not evoke memories.
In Experiment 2b, I used a neuropsychological approach to test the prediction that neural regions underlying music-evoked emotions are also critical for MEAMs. I tested the hypothesis that individuals with damage to brain regions important for music-evoked emotions (mPFC, amygdala, and striatum) would have impaired MEAMs. Individuals with damage to these regions, brain-damaged comparison subjects (with damage to other regions) and neurologically normal comparison subjects completed the same task as in Experiment 2a. The results indicated partial support for the hypothesis, showing that individuals with mPFC, but not striatal, damage had slightly decreased MEAM vividness. Additionally, individuals with damage to the striatum and mPFC showed a disconnect between emotional ratings and physiological responsiveness.
These findings provide important implications for the use of music in therapeutic settings. Since musical reward is predominantly preserved in individuals with brain damage, music can be used to improve mood and affect in clinical populations. In addition, these findings support the use of music as a memory aid in patients with dementia, since music-evoked memories are shown to be more vivid than memories evoked by other cues. Together, these experiments provide partial support for the hypothesis that neural regions important for emotion are also critical for MEAMs, indicating that emotion may be an important aspect underlying music-evoked autobiographical memories.